Recent studies in tree shrew, a mammal closely related to primates, and in other species suggest that a mechanism normally operates during ocular development to coordinate the axial length of the eye with the focal length provided by the cornea and lens, producing emmetropia. Disruption of this mechanism with deprivation of visual forms results in an elongated, myopic eye. The goal of this project is to understand the mechanism that normally guides developing eyes toward emmetropia. The proposed experiments will explore three questions that derive from our past work on emmetropization: 1) what type of retinal signal(s) may be produced by defocussed images on the retina, 2) how do the signal(s) for control of ocular elongation cross from the retina via the choroid to the sclera and 3) how is the sclera remodelled to control elongation of the eye? Specifically, we will: 1) test our hypothesis that the emmetropization mechanism in tree shrew is a"1-way" mechanism able only to detect defocus and not a "2-way" mechanism able to differentiate between "myopic defocus" (focal plane in front of the retina) and "hyperopic defocus" (focal plane behind the retina), 2) investigate whether there are changes in choroidal blood flow in deprived myopic eyes that might participate in the communication of signals from retina to sclera and 3) examine mechanical, morphological and biochemical changes in the sclera that occur during normal development, induced myopia and recovery from myopia. The proposed experiments will significantly advance our understanding of the emmetropization mechanism. This, in turn, can help us to learn how human emmetropization normally occurs and how disruptions in the emmetropization mechanism may lead to human myopia and hyperopia.